© The Author 2006. Published by Oxford University Press.
CORRESPONDENCE |
Re: Carbonated Soft Drink Consumption and Risk of Esophageal Adenocarcinoma
Correspondence to: Mohandas K. Mallath, MD, Department of Digestive Diseases and Clinical Nutrition, Tata Memorial Hospital, Parel, Mumbai 400012, India (e-mail: mohandaskm{at}vsnl.net).
In the recent study by Mayne et al. (1), consumption of carbonated soft drinks (CSD) was positively associated with gastroesophageal reflux (GER) and inversely associated with adenocarcinoma of the esophagus. Likewise, in 1997, this study group had reported statistically significantly reduced risks for adenocarcinoma of the esophagus in wine drinkers (odds ratio [OR] = 0.6, 95% confidence interval [CI] = 0.5 to 0.8) and attributed this to sampling bias or residual confounding (2). The reduced risks for adenocarcinoma of the esophagus in CSD drinkers could be attributed to similar reasons as discussed below.
First, the control subjects were younger than the case patients having adenocarcinoma of the esophagus (2). There were 124 case patients and 357 control subjects aged 64 or less years and 169 case patients and 338 control subjects aged 65 or more years (P = .009) (2). The Continuing Survey of Food Intakes by Individuals reported large differences in CSD by age (3). Total CSD intakes in young (40–59 years) and old (60 years and older) White males were 374 g/day and 144 g/day, respectively (3). Mayne et al. also found statistically significantly higher consumption of CSD in younger than in older control subjects (1).
Second, the control subjects had statistically significantly higher income (Ptrend = .005) than the case patients with adenocarcinoma of the esophagus (2). The Continuing Survey of Food Intakes by Individuals reported large differences in CSD consumption by income (4). For example, the daily diet-CSD intakes among men aged 40–59 years were 53 g/day, 80 g/day, and 139 g/day in subjects with incomes 131%, 131%–350%, and greater than 350% of the poverty line, respectively (4). Mayne et al. found an increasing trend in total CSD consumption in the control subjects with higher income (1). The consumption of diet CSD by income groups is not discussed.
Third, the duration of CSD consumption is missing from this study (1). CSD consumption was ascertained for 3 to 5 years before the diagnosis of cancer (1,2,5). It was hypothesized that CSD contribute to the development of adenocarcinoma of the esophagus by inducing GER for several decades (6). The U.S. per capita trends show that rise in CSD consumption preceded the rise of adenocarcinoma of the esophagus by 20 years or more (6). People with heartburn for 20 or more years have the highest risk for adenocarcinoma of the esophagus (5,7). Stratification by GER symptoms cannot replace the duration of CSD intake in the decades prior to the diagnosis of cancer. This limitation is brought out in another publication of theirs (5). Ever having used H2 blockers was not associated with esophageal adenocarcinoma risk (OR = 0.9, 95% CI = 0.5 to 1.5); the odds ratio was 1.3 (95% CI = 0.6 to 2.8) in long-term (4 or more years) users but increased to 2.1 (95% CI = 0.8 to 5.6) when used in the 5 years before the interview (5).
The question of public health relevance is whether high school students and young adults can drink several cans of CSD everyday for many decades without increasing the lifetime risk of GER disease (GERD) and adenocarcinoma of the esophagus. More epidemiologic studies are therefore needed to provide the answer. Maine et al. report more frequent self-reported reflux symptoms in participants who consumed more CSD (1). Therefore, CSD could be a new risk factor for GERD, the prevalence of which is rising rapidly.
REFERENCES
(1) Mayne ST, Risch HA, Dubrow R, Chow WH, Gammon MD, Vaughan TL, et al. Carbonated soft drink consumption and risk of esophageal adenocarcinoma. J Natl Cancer Inst 2006;98:72–5.
(2) Gammon MD, Schoenberg JB, Ahsan H, Risch HA, Vaughan TL, Chow WH, et al. Tobacco, alcohol and socioeconomic status and adenocarcinomas of the esophagus and gastric cardia. J Natl Cancer Inst 1997;89:1277–84.
(3) U.S. Department of Agriculture, Agricultural Research Service. August 1998. Data tables: food and nutrient intakes by race, 1994–96. Available at: http://www.ars.usda.gov/SP2UserFiles/Place/12355000/pdf/Race.PDF. [Last accessed: January 23, 2005.]
(4) U.S. Department of Agriculture, Agricultural Research Service. August 1998. Data tables: food and nutrient intakes by income, 1994–96. Available at: http://www.ars.usda.gov/SP2UserFiles/Place/12355000/pdf/Income.PDF. [Last accessed: January 23, 2005.]
(5) Farrow DC, Vaughan TL, Sweeney C, Gammon MD, Chow WH, Risch HA, et al. Gastroesophageal reflux disease, use of H2 receptor antagonists, and risk of esophageal and gastric cancer. Cancer Causes Control 2000;11:231–38.[CrossRef][ISI][Medline]
(6) Mallath MK. Rise of esophageal adenocarcinoma in USA is temporally associated with the rise in carbonated soft drink consumption. Gastroenterology 2004;126(Suppl 2):A619.
(7) Lagergren J, Bergström R, Lindgren A, Nyrén O. Symptomatic gastroesophageal reflux is a strong risk factor for esophageal adenocarcinoma. N Engl J Med 1999;340:825–31.
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J Natl Cancer Inst 2006 98: 646-647.
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